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Pharm II Unit II > Diuretics > Flashcards

Diuretics Flashcards

1
Q

Conditions that promote the development of edema

A

Altered blood circulation (inc arterial or venous pressure)

Altered blood composition (dec osmotic gradient, salt and water retention)

Inadequate lymphatic drainage

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2
Q

Diseases often associated with edema

A

HF

Hepatic cirrhosis

Nephritis, nephrosis, renal damage due to HTN

Diseases involving increased steroid hormone secretion

Pre-eclampsia, toxemia

Hypersensitivity reactions (anaphylaxis)

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3
Q

_____% of all fluid filtered by the glomerulus is reabsorbed

A

> 99%

Anything <43kD is filtered

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4
Q

_____% of Na+ is reabsorbed in the proximal tubule

A

65%

H+ and Na+ via active transport - NaK ATPase

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5
Q

What diuretics work in the proximal tubule?

A

Acetazolamide (diamox)

Osmotic diuretics

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6
Q

What occurs in the loop of Henle?

A

Passive H2O reabsorption —> concentration of urine

NOTE - the loop of Henle is thinner b/c this portions need lots of mitochondria to produce energy for ACTIVE transport

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7
Q

What diuretics work on the loop of Henle?

A

Osmotic diuretics

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8
Q

What exchanges occur in the thick ascending limb of LOH?

A

Active reabsorption of K+, 2Cl-, Na+

Passive reabsorption of K+, Ca2+, Mg2+, Na+

25% of Na+ is reabsorbed here, but no H2O

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9
Q

What diuretics work on the thick ascending limb of LOH?

A

LOOP diuretics

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10
Q

What occurs in the early distal tubule?

A

Reabsorption of NaCl (not H2O) by active transport

4-8% of total Na+ reabsorption occurs here

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11
Q

What diuretics work in the early distal tubule?

A

Thiazides

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12
Q

What occurs in the late distal tubule?

A

Ca2+ reabsorption

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13
Q

What occurs in the collecting duct?

A

K+ and H+ excretion (via Na+/K+ and Na+/H+ exchange)

NaCl reabsorption by aldosterone

H2O reabsorption by ADH

Some K+ and H+ independent of aldosterone

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14
Q

What diuretics work on the collecting duct?

A

Aldosterone antagonists (by inhibiting NaCl reabsorption)

ADH antagonists (by inhibiting H2O reabsorption)

Osmotic diuretics

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15
Q

Where does potassium reabsorption and secretion occur?

A

Reabsorption in proximal tubule (CANNOT be influenced by drugs)

Secretion in late distal tubule and collecting duct
• Exchange of Na+ with K+, with or w/o aldosterone
• Can be modified by aldosterone antagonists and K+ sparing diuretics

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16
Q

What affects reabsorption of Calcium and Magnesium occur?

A

Thiazides diuretics —> increase Ca2+ reabsorption

Loop diuretics —> increased Ca2+ and Mg2+ excretion

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17
Q

The rate of diffusion of organic compounds depends upon…

A

Lipid solubility, pKa, and pH

Weak acids at low pH will remain mostly unionized (lipid soluble) and are easily diffusible across the epithelium and vice-versa

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18
Q

What do we need to know about uric acid?

A

It’s secreted and reabsorbed by carrier dependent mechanisms

ACID DRUGS will compete for uric acid excretion —> gouty attack

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19
Q

What drugs are carbonic anhydrase inhibitors?

A

Acetazolamide (Diamox)
Dorzolamide (Truspot)
Brinzolamide (Azopt)

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20
Q

MOA for carbonic anhydrase inhibitors

A

Inhibits carbonic anhydrase enzyme

Blocks H2CO3 production

Decreases H+ for exchange with Na+, resulting in increased Na+ and H2O loss

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21
Q

What are the indications for carbonic anhydrase inhibitors?

A

GLAUCOMA (that’s why two of the drugs are eye drops) —> inhibition of bicarbonate transport in the eye and the chorionic plexus —> decreased aqueous humor and CSF

Alkalinization of the urine

Metabolic ALKALOSIS due to acute mountain sickness

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22
Q

Why are CA inhibitors not used as a regular diuretic?

A

Their effectiveness decreases after several days b/c metabolism —> build up of H+

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23
Q

Adverse effects of CA inhibitors

A

HYPERCHLOREMIC METABOLIC ACIDOSIS b/c the Na+ is in the form of NaHCO3 and not NaCl

Hypokalemia (b/c inc Na+ in lumen —> inc Na+/K+ exchange in DCT)

Renal stones (b/c inc PO4 and Ca2+ in urine)

HYPERURICEMIA b/c they are acids and compete for uric acid excretion

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24
Q

Contraindications for CA inhibitors

A

Hepatic cirrhosis (from dec ammonia excretion)

Sulfa hypersensitivity

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25
What drugs are Loop Diuretics?
Furosemide (Lasix) Bumetanide Torsemide Ethacrynic acid
26
MOA for Loops
Block the NaK2Cl co-transporter**** —> inc Na+ in lumen =—> diuresis Induce kidney prostaglandins —> reduced salt transport in kidney and VASODILATION
27
Loops still work for diuresis in patients with _______ when other diuretics will not
Low GFR
28
Indications for Loops
HF (b/c they move large amounts of water) PULMONARY EDEMA - relieves pulmonary congestion by increasing systemic venous capacitance Severe refractory peripheral edema HYPERCALCEMIA (b/c dec reabsorption of Mg2+ and Ca2+ by reducing K+ gradient)
29
Pharmacokinetics of loops
Oral or parenteral (for faster action) Renal excretion
30
Adverse effects of Loops
High potency —> electrolyte imbalance HYPOKALEMIC METABOLIC ALKALOSIS (b/c induces K+ and H+ loss at the DCT) Hypochloremia HYPOCALCEMIA HYPOMAGNESESMIA HYPERURICEMIA GI upset IRREVERSIBLE OTOTOXICITY
31
All looks are ototoxic but ______ is the worst
Ethacrynic acid
32
Ototoxic effects of loops are worse when given concurrently with...
Aminoglycosides
33
Contraindications for Loops
SULFA hypersensitivity (EXCEPT ETHACRYNIC ACID) Drug interactions • COX inhibitors interfere with its action • Aminoglycosides (ototoxicity) • Lithium (loss of Na+ increases Li+ retention —> toxicity) • Digoxin (loss of K+ —> toxicity) ``` Overzealous use is dangerous in • Hepatic cirrhosis • Borderline renal failure • HF (We use them still but very carefully) ```
34
What makes Ethacrynic acid special?
MOA the same and adverse effects are similar to Lasix BUT It’s not a sulfonamide so it can be used in pt with sulfa allergy It has the highest risk of ototoxicity
35
What drugs are thiazides diuretics?
Hydrochlorothiazide*** Chlorothiazide ``` Related compounds: Chlorthalidone Metolazone Quinethazone Indapamide ```
36
Which diuretics are the most widely used?
Thiazides
37
MOA for thiazides
Inhibition of sodium resorption at the early distal tubule via inhibition of the Na-Cl cotransporter Effect is dependent on PG synthesis
38
Main clinical indications for thiazides
HYPERTENSION HF (not as effective at reducing edema as loops but can start them on a loop and then switch to HCTZ for maintenance) Nephrolithiasis Nephrogenic diabetes insipidus
39
What are the beneficial and adverse effects of the ATP-dependent K+ channels opened by thiazides —> hyperpolarization of cell membranes
Beneficial: relaxation of smooth muscle cells —> VASODILATION Adverse: REDUCED INSULIN SECRETION
40
What are the indications for Thiazides?
Lower systemic BP and enhance the anti-HTN action of other drugs (ACE-I, ARBs, ß-blockers) Decrease Ca2+ excretion by increasing activity of PTH-dependent Ca2+ channels (not b/c of PTH but b/c inc luminal Na+) NOT effective in osteoporosis May be beneficial in renal calculosis
41
What’s special about thiazide pharmacokinetics?
Oral, well-absorbed Secreted by the organic acid secreting system —> COMPETES WITH URIC ACID
42
How is Chlorthalidone different from other thiazides?
Slowly absorbed, therefore appears to have longer duration Therefore PREFERRED b/c it has the best pharmacokinetics of the class
43
How is Indapamide different from other thiazides?
Excreted by the biliary system, therefore is useful in patients with RENAL INSUFFICIENCY
44
Adverse effects of thiazides
Dizziness, weakness, fatigue, leg cramps common HYPOKALEMIC METABOLIC ALKALOSIS*** b/c of K+ and H+ loss at the DCT HYPERURICEMIA*** MAGNESIUM LOSS Iodide and Bromide loss HYPERGLYCEMIA*** May dec release of insulin and inc glucose intolerance ELEVATED SERUM LIPID LEVELS
45
Which thiazide is the exception to the rule of thiazides increasing serum lipid levels?
Indapamide
46
Contraindications of thiazides
SULFA HYPERSENSITIVY (may be inhibited by NSAIDs) HYPOKALEMIA can precipitate digitalis toxicity (arrhythmias) and hepatic coma in CIRRHOTIC patients HYPERGLYCEMIA and carb intolerance may occur in DIABETICS HYPERURICEMIA so don’t give to someone with GOUT HYPONATREMIA if too hydrated HYPERCALCEMIA with latent primary HYPERPARATHYROIDISM LITHIUM TOXICITY b/c Li clearance reduced
47
What is unique about Metolazone
Able to produce diuresis in patients with a reduced GFR Loop diuretics can work at low GFR but most thiazides don’t, except METOLAZONE
48
What is unique about Indapamide?
3 major differences from other thiazides: 1. Causes pronounced vasodilation (Ca2+ channel blocker) 2. DOES NOT increase plasma lipids**** 3. Metabolized in the liver and kidney 50/50****
49
What are the two classes of potassium sparing diuretics?
Aldosterone antagonists Direct inhibitors of Na+ flux
50
How do potassium sparing diuretics work in general?
Interfere with Na+ reabsorption at the distal exchange site —> permits loss of Na+ and H2O and cause conservation of K+ WEAK diuretics compared to thiazides/loops Reduce K+ loss and alkalosis by other diuretics Used IN COMBO with other K+ losing drugs
51
MOA for Aldosterone Antagonists
Competitive inhibition of aldosterone High doses —> inhibits glucocorticoid and sex hormone receptors Aldosterone inhibition promotes the excretion of Na+ and retention of K+ at the DCT • Less Na+ channels, blocked Na+ conductance, reduced K+ excretion
52
What is the prototype aldosterone antagonist?
Spironolactone
53
What are the indication for Spironolactone?
Edema associated with HF, cirrhosis, and nephrotic syndrome (in combo) Most effective drug for treating HYPERALDOSTERONISM HIRSUTISM (androgen receptor antagonist)
54
Adverse effects of spironolactone
GYNECOMASTIA (b/c androgen receptor antagonist) ``` Occasional HYPERKALEMIA (usually only when in combo) • Use with caution with ACE/ARBs ```
55
Contraindications for Spironolactone
Hyperkalemia (burn patients) Chronic renal insufficiency Liver damage, hyperchloremic acidosis may occur in these patients
56
How is Eplerenone (Inspra) different from Spironolactone?
Selective aldosterone receptor antagonist Has the same effects as Spironolactone except... Decreased endocrine related side effects (NO MAN BOOBS) Metabolized by CYP3A4 —> drug interactions
57
What is the MOA for Amiloride and Triamterene?
Inhibit the Na+/K+ ion exchange mechanism INDEPENDENT OF ALDOSTERONE by directly inhibiting the aldosterone-sensitive Na+ channel Leads to a decreased K+ excretion
58
Indications for Amiloride/Triamterene
Combo with K+ losing diuretics (weak diuretic effect on their own) NO HYPERURICEMIA b/c they are not acids*** The only diuretic class that are not
59
DOC for Li+ induced diabetes insipidus
Amiloride
60
Adverse effects of potassium sparing diuretics
HYPERKALEMIA in chronic use or combo with other potassium sparing agents
61
In whom are potassium sparing diuretics contraindicated
Burn patients (b/c prone to hyperkalemia)
62
Examples of Osmotic diuretics
Mannitol Isosorbide Glycerin Urea ***All are IV only (give diarrhea if given orally)
63
MOA for osmotic diuretics
Keeps water in the tubules Produce water diuresis (not dependent upon sodium)
64
Indications for Osmotic Diuretics
IV ONLY - very specialized use Prophylaxis for ACUTE RENAL FAILURE Reduce intraocular pressure prior to eye surgery Reduce intracranial pressure in pt with brain edema Protect kidney against nephrotoxic substances
65
Adverse effects of osmotic diuretics
HA, N/V***, chills, dizziness, polydipsia, lethargy, confusion, chest pain (basically dehydration symptoms) Excessive administration —> extracellular volume expansion** PULMONARY EDEMA IN HF (CONTRAINDICATION) EXCESSIVE CELLULAR DEHYDRATION
66
Tell me all there is to know about Desmopressin
Synthetic ADH Activates V2>>V1 receptors Used to treat CENTRAL DIABETES INSIPIDUS Acts to decrease H2O excretion Can be given Oral, IV, SC, or intranasal Side fx: • GI, HA, Allergy, HYPOnatremia
67
What drugs are ADH antagonists?
Conivaptan*** Tolvaptan Demeclocycline (FYI - for SIADH) Lithium (FY)
68
What’s special about Conivaptan?
IV ONLY Adverse effects: • HYPOKALEMIA • Injection site rxn • Orthostatic hypotension, a fib, hypotension Contraindications: Hyponatremia associated with HYPOVOLEMIA
69
How is Tolvaptan different from Conivaptan?
Non-peptide V2 vasopressin receptor antagonist Administered orally Initiated and re-initiated in a hospital and then continued on an outpatient basis
70
What happens when you combine loops and thiazides?
May produce diuresis when none of them is effective alone
71
What happens when you combine potassium sparing diuretics and loops or thiazides?
May balance out potassium losses
72
Put the diuretics in order of maximum diuretic effect
Loop >> thiazides >> [CA inhibitors] > K+ sparing **CA inhibitors only work for a few days

Pharm II Unit II (8 decks)

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